0022-534 7/79/1216-0783$02. 00/0 Vol. 121, June
THE JOURNAL OF UROLOGY
Copyright © 1979 by The Williams & Wilkins Co.
Printed in U.S.A.
URETHRAL HYPOTONICITY AFTER SUPRASACRAL SPINAL CORD INJURY JEFFREY R. WOODSIDE
AND
EDWARD J. MCGUIRE
From the Divisions of Urology, Departments of Surgery, University of New Mexico School of Medicine, Albuquerque, New Mexico, and Yale University School of Medicine, New Haven, Connecticut
ABSTRACT
Established suprasacral spinal cord injuries usually are associated with detrusor hyperreflexia and varying degrees of detrusor-sphincter dyssynergia. Occasionally, such injuries result in detrusor areflexia or urethral hypotonicity or both. The results of the urodynamic evaluation of 4 patients with suprasacral spinal cord injuries are described. Detrusor areflexia and urethral hypotonicity were demonstrated in 3 cases and urethral smooth muscular hypotonia but preserved reflex detrusor function in 1. It is shown that destruction of the thoracolumbar sympathetic outflow can cause the complete loss of urethral smooth muscular closing function and that resting urethral closure is totally independent ofpreganglionic cholinergic influences. Trauma to the spinal cord above the conus medullaris (upper motor neuron lesion) is followed by a variable period of spinal shock during which there is detrusor areflexia. After resolution of spinal shock the spinal cord below the level of injury is released from higher control and, typically, the previously areflexic detrusor becomes hyperreflexic and is accompanied by varying degrees of detrusor-sphincter dyssynergia. Thus, reflex micturition with incontinence is established. Although occasionally reported, it is not generally appreciated that established suprasacral spinal cord injuries can result in either detrusor areflexia or urethral hypotonicity or both. 1, 2 Herein we describe the urodynamic results in 4 patients in whom urethral pressure profile determinations, external urethral sphincter electromyographic studies and simultaneous bladder and urethral pressures with fluoroscopic voiding cystourethrography3 were done. The etiology of these unusual findings and the management of the resultant voiding dysfunction are discussed. CASE REPORTS
Case 1 . An 8-year-old Indian boy was run over by a tractor 6 years earlier and suffered a complete T5 paraplegia. He had continuous urinary incontinence. Physical examination showed a T5 sensory level, flaccid paraplegia and negative Babinski's signs. The external anal sphincter was atonic and the bulbocavernosus reflex was absent. Urodynamic investigation revealed nearly absent sphincter electromyographic activity (figs. 1 and 2). The urethral pressure profile with the bladder empty was 20 cm. water from the bladder neck to the external meatus. With bladder filling the urethral and bladder pressures increased to 28 cm. water, at which time urine loss occurred. The Crede maneuver resulted in a loss of positive urethral closing pressure, an isobaric urethra and bladder, and a completely empty bladder. The patient currently is managed by Crede's maneuver every 3 hours and has complete interval continence. Case 2. A 42-year-old Spanish American man fell from a truck 3 years earlier and suffered a TlO on Tll fracturedislocation with a resultant complete TlO paraplegia. He was treated initially with an indwelling Foley catheter for 18 months and a large, pendulous, urethral diverticulum developed at the penoscrotal junction. He was then treated with clean intermittent self-catheterization. Physical examination Accepted for publication September 15, 1978.
showed a TlO sensory level, flaccid paraplegia and negative Babinski signs. The external anal sphincter was flaccid and the bulbocavernosus reflex was absent. Urodynamic evaluation showed little sphincter electromyographic activity (fig. 3). Urethral pressure profile with the bladder empty was 17 cm. water throughout the entire urethra and did not increase with bladder filling. At 60 ml. bladder volume the urethral and bladder pressures became equal and urine loss occurred. Further filling resulted in continuous urine loss. The patient was then treated by condom catheter drainage and the Crede maneuver. Case 3. A 62-year-old man had sudden paraplegia with a TS sensory level thought to be the result of a vascular occlusion. Two months after the onset of the paralysis constant urinary incontinence occurred. Urodynamic evaluation showed a hyperreflexic bladder with a sudden intravesical pressure elevation at a 100 ml. bladder volume. Resting urethral profilometry disclosed no proximal urethral closing pressure but normal pressure in the area of the membranous urethra associated with external sphincter electromyographic activity. With the onset of detrusor contractile activity, external sphincter activity increased markedly (fig. 4). Case 4. G. F., a 32-year-old man, had flaccid paraplegia with a T3 sensory level after an acute viral illness. Urodynamic evaluation showed a gradual increase in intravesical pressure with filling with the vesical outlet closed by a large balloon Foley catheter. There was no effective urethral closing pressure measured by the profile maneuver and no external sphincter electromyographic activity (fig. 5). The bulbocavernosus reflex was negative and no reflex detrusor contractile activity occurred with filling to 800 ml. DISCUSSION
Thoracolumbar sympathetic nuclei at the Tll to L2 spinal cord level supply neurons to the hypogastric nerve which innervate the bladder and urethra. The conus medullaris contains the sacral cord segments and lies opposite the Ll-L2 intervertebral space. The detrusor and pudendal nuclei arise from 82, 83 and 84 and give origin, respectively, to the preganglionic parasympathetic fibers to the detrusor and the lower motor neurons of the pudenda} nerve supplying the striated external urethral sphincter. Trauma to the conus medullaris or cauda equina (lower motor neuron lesion) results in detrusor areflexia, urinary retention and urinary incontinence. 783
784
WOODSIDE AND MCGUIRE
A
C
EMG
EMG
30[-::-~\-+--•...--..~~,....,-~Y-CMS HzO
100
X
200
~U==:::=:::::::::=i---__________ ________
_B
.._
100ml
50
300ml X
__,
X
Fm. 1. Pelvic floor electromyogram (EMG), urethral pressure (U) and bladder pressure (Bl recordings from case 1. Bladder filling to 300 ml. shows increasing bladder pressure but no detrusor contraction. Electromyographic activity is minimal.
B
Fm. 3. Case 2. A, urodynamic recordings show minimal electromyographic activity. Bladder and urethral pressures become equal at 60 ml. bladder volume. B, tracing of radiogram exposure at X below bladder tracing reveals widely patent proximal urethra.
B
Fm. 2. Case 1. A, tracing of radiogram (X on left side of figure 1) shows widely patent urethra during Crede's maneuver, at which time urethral and bladder pressures are equal. B, tracing of radiogram (X on right side of figure 1) reveals filling of posterior urethra when bladder pressure just exceeds static urethral pressure. The results of urodynamic evaluation in these patients are at variance with the usual findings after suprasacral spinal cord injury. Detrusor areflexia, preservation of detrusor tonic response to filling and urethral hypotonia were noted in 3 patients, while 1 showed urethral smooth muscular hypotonia but preserved reflex detrusor function. The active components of urethral resistance include smooth and skeletal musculature. Smooth muscular tone is thought to be at least partially under sympathetic control. Injuries to the cauda equina or sacral cord segments commonly result in detrusor and external sphincter denervation but preservation of smooth muscular urethral closing function. 4 Thus, the loss of reflex detrusor and perineal floor electromyographic activity seen in 3 of these patients, all with primary injuries superior to the sacral cord segments, implies extension of the spinal cord injury to involve the sacral segments. The deficit in urethral smooth muscular closing function associated with a wide open bladder neck and proximal urethra is indicative of an extensive injury to the thoracolumbar spinal cord with loss ~f preganglionic
EMG - . . . .. . 4 .......
x,
.... x,
•.. • ..•
Fm. 4. Simultaneous recording of urethral pressure at 4 cm.
(U
4 cm.) from bladder neck, intravesical pressure (Bl and external
urethral sphincter electromyography during bladder filling to 300 ml. bladder volume in case 3. Note increase in urethral pressure with filling associated with increase in perinea! floor electromyographic activity, which persists after onset of detrusor contraction that is seen as elevation in intravesical pressure. There is incomplete suppression of external sphincter electromyographic activity and some voiding at mid point of detrusor pressure increase. Inset tracings were made from radiograms exposed at points X1 and X2 below electromyographic tracing and show wide open prostatic urethra at rest with closure of urethra seen in area of membranous urethra and no essential change in configuration on tracing of radiogram made at mid point of detrusor contraction. Study reveals reflex detrusor activity and sphincter hyperreflexia but widely patulous bladder neck at rest. sympathetic motor activity. In all of the patients studied the superior level of spinal cord injury was cranial to the thoracolumbar sympathetic outflow. The fourth patient demonstrated absence of urethral smooth muscular closing function but had reflex detrusor activity and hyperreflexic external sphincter activity. The latter 2 findings indicate an intact sacral cord. Therefore, the neurologic lesion
URETHRAL HYPOTONICITY AFTER SUPRASACRAL SPINAL CORD INJURY
785
innervation of the urethral smooth musculature.&-8 The fact that this activity may be modified by a parasympathetic discharge does not preclude the importance of adrenergic influences on the lower urinary tract. 9 The management of these patients is dependent on the degree of continence that is related to the balance between bladder tone with filling and urethral resistance. In patients with preservation of reasonable bladder capacity intermittent catheterization or the Crede maneuver is a satisfactory method. In male subjects with smaller capacity and poor urethral pressures external condom catheter drainage is more effective. In female subjects with low bladder capacity and continuous incontinence management by either of these techniques is unsuitable since loss of urethral smooth muscular function virtually precludes continence. X
REFERENCES
FIG. 5. Simultaneous urethral (U) and bladder (B) pressures and external urethral sphincter electromyography recording during bladder filling in case 4. Urethral closing pressure is low and is quickly overcome by intravesical pressure at 30 ml. bladder volume. At volumes >30 ml. urinary leakage is continuous. Electromyographic recordings show virtually no activity. Inset tracings reveal wide open active urethra including area of membranous urethra.
1. Thomas, D. G., Smallwood, R. and Graham, D.: Urodynamic
2. 3.
must involve an extensive destruction of the lower thoracic and lumbar cord associated with loss of sympathetic activity, yet the sacral cord segments must be intact as shown by the reflex detrusor-sphincter dyssynergia. These findings have important clinical and theoretical implications. Anatomical studies have not demonstrated a-adrenergic terminals to be distributed widely in the urethra of male subjects except in the area of the preprostatic urethra and in female subjects they have not been found at all. 5 In part, because of this finding, it has been suggested that parasympathetic activity is responsible for urethral smooth muscular closure. The lack of an adverse effect of sympathectomy on lower urinary tract function has been cited as further evidence that sympathetic activity is oflittle importance in lower urinary function. The demonstration that urethral smooth muscular closing function can be completely lost after extensive spinal cord injury involving the thoracolumbar sympathetic outflow indicates that urethral smooth muscular function is not autonomous and requires neural input. However, this neural participation in urethral function is unlikely to be parasympathetic in nature, since urethral functional loss was not influenced by the preservation or loss of sacral reflex activity. Indeed, the loss of urethral smooth muscular closing function in a patient with preservation of parasympathetically mediated detrusor reflex activity is strong evidence that resting urethral closure is totally independent of cholinergic influences. These findings have been duplicated experimentally and an extensive body of evidence supports the concept of sympathetic
4. 5. 6. 7.
8. 9.
observations following spinal trauma. Brit. J. Urol., 47: 161, 1975. Yalla, S. V., Blunt, K. J., Fam, B. A., Constantinople, N. L. and Gittes, R. F.: Detrusor-urethral sphincter dyssynergia. J. Urol., 118: 1026, 1977. McGuire, E. J., Wagner, F. and Weiss, R. M.: Treatment of autonomic dysreflexia with phenoxybenzamine. J. Urol., 115: 53, 1976. McGuire, E. J., Diddel, G. and Wagner, F., Jr.: Balanced bladder function in spinal cord injury patients. J. Urol., 118: 626, 1977. Gosling, J. A., Dixon, J. S. and Lendon, R. G.: The autonomic innervation of the human male and female bladder neck and proximal urethra. J. Urol., 118: 302, 1977. McGuire, E. J. and Herlihy, E.: The influence of urethral position on urinary continence. Invest. Urol., 15: 205, 1977. Awad, S. A. and Downie, J. E.: The effect of adrenergic drugs and hypogastric nerve stimulation on the canine urethra. A radiologic and urethral pressure study. Invest. Urol., 13: 298, 1976. Khanna, 0.: Disorders ofmicturition: neuropharmacologic basis and results of drug therapy. Urology, 8: 316, 1976. Saum, W. R. and De Groat, W. C.: Parasympathetic ganglia: activation of an adrenergic inhibitory mechanism by cholinomimetic agents. Science, 175: 659, 1972. EDITORIAL COMMENT
Although the conclusions of this well conducted study are based on a limited number of cases they add valuable information to our understanding of the dual role of sympathetic-parasympathetic systems in the activity of respective urethral profile components. The main statement that "resting urethral closure is totally independent of cholinergic influences" would deserve further investigation to reassess the validity of the theory that claims a cholinergic inhibitory modulating effect upon urethral smooth musculature. A.B.R.
THE JOURNAL OF UROLOGY
Copyright © 1979 by The Williams & Wilkins Co.
Printed in U.S.A.
URETHRAL HYPOTONICITY AFTER SUPRASACRAL SPINAL CORD INJURY JEFFREY R. WOODSIDE
AND
EDWARD J. MCGUIRE
From the Divisions of Urology, Departments of Surgery, University of New Mexico School of Medicine, Albuquerque, New Mexico, and Yale University School of Medicine, New Haven, Connecticut
ABSTRACT
Established suprasacral spinal cord injuries usually are associated with detrusor hyperreflexia and varying degrees of detrusor-sphincter dyssynergia. Occasionally, such injuries result in detrusor areflexia or urethral hypotonicity or both. The results of the urodynamic evaluation of 4 patients with suprasacral spinal cord injuries are described. Detrusor areflexia and urethral hypotonicity were demonstrated in 3 cases and urethral smooth muscular hypotonia but preserved reflex detrusor function in 1. It is shown that destruction of the thoracolumbar sympathetic outflow can cause the complete loss of urethral smooth muscular closing function and that resting urethral closure is totally independent ofpreganglionic cholinergic influences. Trauma to the spinal cord above the conus medullaris (upper motor neuron lesion) is followed by a variable period of spinal shock during which there is detrusor areflexia. After resolution of spinal shock the spinal cord below the level of injury is released from higher control and, typically, the previously areflexic detrusor becomes hyperreflexic and is accompanied by varying degrees of detrusor-sphincter dyssynergia. Thus, reflex micturition with incontinence is established. Although occasionally reported, it is not generally appreciated that established suprasacral spinal cord injuries can result in either detrusor areflexia or urethral hypotonicity or both. 1, 2 Herein we describe the urodynamic results in 4 patients in whom urethral pressure profile determinations, external urethral sphincter electromyographic studies and simultaneous bladder and urethral pressures with fluoroscopic voiding cystourethrography3 were done. The etiology of these unusual findings and the management of the resultant voiding dysfunction are discussed. CASE REPORTS
Case 1 . An 8-year-old Indian boy was run over by a tractor 6 years earlier and suffered a complete T5 paraplegia. He had continuous urinary incontinence. Physical examination showed a T5 sensory level, flaccid paraplegia and negative Babinski's signs. The external anal sphincter was atonic and the bulbocavernosus reflex was absent. Urodynamic investigation revealed nearly absent sphincter electromyographic activity (figs. 1 and 2). The urethral pressure profile with the bladder empty was 20 cm. water from the bladder neck to the external meatus. With bladder filling the urethral and bladder pressures increased to 28 cm. water, at which time urine loss occurred. The Crede maneuver resulted in a loss of positive urethral closing pressure, an isobaric urethra and bladder, and a completely empty bladder. The patient currently is managed by Crede's maneuver every 3 hours and has complete interval continence. Case 2. A 42-year-old Spanish American man fell from a truck 3 years earlier and suffered a TlO on Tll fracturedislocation with a resultant complete TlO paraplegia. He was treated initially with an indwelling Foley catheter for 18 months and a large, pendulous, urethral diverticulum developed at the penoscrotal junction. He was then treated with clean intermittent self-catheterization. Physical examination Accepted for publication September 15, 1978.
showed a TlO sensory level, flaccid paraplegia and negative Babinski signs. The external anal sphincter was flaccid and the bulbocavernosus reflex was absent. Urodynamic evaluation showed little sphincter electromyographic activity (fig. 3). Urethral pressure profile with the bladder empty was 17 cm. water throughout the entire urethra and did not increase with bladder filling. At 60 ml. bladder volume the urethral and bladder pressures became equal and urine loss occurred. Further filling resulted in continuous urine loss. The patient was then treated by condom catheter drainage and the Crede maneuver. Case 3. A 62-year-old man had sudden paraplegia with a TS sensory level thought to be the result of a vascular occlusion. Two months after the onset of the paralysis constant urinary incontinence occurred. Urodynamic evaluation showed a hyperreflexic bladder with a sudden intravesical pressure elevation at a 100 ml. bladder volume. Resting urethral profilometry disclosed no proximal urethral closing pressure but normal pressure in the area of the membranous urethra associated with external sphincter electromyographic activity. With the onset of detrusor contractile activity, external sphincter activity increased markedly (fig. 4). Case 4. G. F., a 32-year-old man, had flaccid paraplegia with a T3 sensory level after an acute viral illness. Urodynamic evaluation showed a gradual increase in intravesical pressure with filling with the vesical outlet closed by a large balloon Foley catheter. There was no effective urethral closing pressure measured by the profile maneuver and no external sphincter electromyographic activity (fig. 5). The bulbocavernosus reflex was negative and no reflex detrusor contractile activity occurred with filling to 800 ml. DISCUSSION
Thoracolumbar sympathetic nuclei at the Tll to L2 spinal cord level supply neurons to the hypogastric nerve which innervate the bladder and urethra. The conus medullaris contains the sacral cord segments and lies opposite the Ll-L2 intervertebral space. The detrusor and pudendal nuclei arise from 82, 83 and 84 and give origin, respectively, to the preganglionic parasympathetic fibers to the detrusor and the lower motor neurons of the pudenda} nerve supplying the striated external urethral sphincter. Trauma to the conus medullaris or cauda equina (lower motor neuron lesion) results in detrusor areflexia, urinary retention and urinary incontinence. 783
784
WOODSIDE AND MCGUIRE
A
C
EMG
EMG
30[-::-~\-+--•...--..~~,....,-~Y-CMS HzO
100
X
200
~U==:::=:::::::::=i---__________ ________
_B
.._
100ml
50
300ml X
__,
X
Fm. 1. Pelvic floor electromyogram (EMG), urethral pressure (U) and bladder pressure (Bl recordings from case 1. Bladder filling to 300 ml. shows increasing bladder pressure but no detrusor contraction. Electromyographic activity is minimal.
B
Fm. 3. Case 2. A, urodynamic recordings show minimal electromyographic activity. Bladder and urethral pressures become equal at 60 ml. bladder volume. B, tracing of radiogram exposure at X below bladder tracing reveals widely patent proximal urethra.
B
Fm. 2. Case 1. A, tracing of radiogram (X on left side of figure 1) shows widely patent urethra during Crede's maneuver, at which time urethral and bladder pressures are equal. B, tracing of radiogram (X on right side of figure 1) reveals filling of posterior urethra when bladder pressure just exceeds static urethral pressure. The results of urodynamic evaluation in these patients are at variance with the usual findings after suprasacral spinal cord injury. Detrusor areflexia, preservation of detrusor tonic response to filling and urethral hypotonia were noted in 3 patients, while 1 showed urethral smooth muscular hypotonia but preserved reflex detrusor function. The active components of urethral resistance include smooth and skeletal musculature. Smooth muscular tone is thought to be at least partially under sympathetic control. Injuries to the cauda equina or sacral cord segments commonly result in detrusor and external sphincter denervation but preservation of smooth muscular urethral closing function. 4 Thus, the loss of reflex detrusor and perineal floor electromyographic activity seen in 3 of these patients, all with primary injuries superior to the sacral cord segments, implies extension of the spinal cord injury to involve the sacral segments. The deficit in urethral smooth muscular closing function associated with a wide open bladder neck and proximal urethra is indicative of an extensive injury to the thoracolumbar spinal cord with loss ~f preganglionic
EMG - . . . .. . 4 .......
x,
.... x,
•.. • ..•
Fm. 4. Simultaneous recording of urethral pressure at 4 cm.
(U
4 cm.) from bladder neck, intravesical pressure (Bl and external
urethral sphincter electromyography during bladder filling to 300 ml. bladder volume in case 3. Note increase in urethral pressure with filling associated with increase in perinea! floor electromyographic activity, which persists after onset of detrusor contraction that is seen as elevation in intravesical pressure. There is incomplete suppression of external sphincter electromyographic activity and some voiding at mid point of detrusor pressure increase. Inset tracings were made from radiograms exposed at points X1 and X2 below electromyographic tracing and show wide open prostatic urethra at rest with closure of urethra seen in area of membranous urethra and no essential change in configuration on tracing of radiogram made at mid point of detrusor contraction. Study reveals reflex detrusor activity and sphincter hyperreflexia but widely patulous bladder neck at rest. sympathetic motor activity. In all of the patients studied the superior level of spinal cord injury was cranial to the thoracolumbar sympathetic outflow. The fourth patient demonstrated absence of urethral smooth muscular closing function but had reflex detrusor activity and hyperreflexic external sphincter activity. The latter 2 findings indicate an intact sacral cord. Therefore, the neurologic lesion
URETHRAL HYPOTONICITY AFTER SUPRASACRAL SPINAL CORD INJURY
785
innervation of the urethral smooth musculature.&-8 The fact that this activity may be modified by a parasympathetic discharge does not preclude the importance of adrenergic influences on the lower urinary tract. 9 The management of these patients is dependent on the degree of continence that is related to the balance between bladder tone with filling and urethral resistance. In patients with preservation of reasonable bladder capacity intermittent catheterization or the Crede maneuver is a satisfactory method. In male subjects with smaller capacity and poor urethral pressures external condom catheter drainage is more effective. In female subjects with low bladder capacity and continuous incontinence management by either of these techniques is unsuitable since loss of urethral smooth muscular function virtually precludes continence. X
REFERENCES
FIG. 5. Simultaneous urethral (U) and bladder (B) pressures and external urethral sphincter electromyography recording during bladder filling in case 4. Urethral closing pressure is low and is quickly overcome by intravesical pressure at 30 ml. bladder volume. At volumes >30 ml. urinary leakage is continuous. Electromyographic recordings show virtually no activity. Inset tracings reveal wide open active urethra including area of membranous urethra.
1. Thomas, D. G., Smallwood, R. and Graham, D.: Urodynamic
2. 3.
must involve an extensive destruction of the lower thoracic and lumbar cord associated with loss of sympathetic activity, yet the sacral cord segments must be intact as shown by the reflex detrusor-sphincter dyssynergia. These findings have important clinical and theoretical implications. Anatomical studies have not demonstrated a-adrenergic terminals to be distributed widely in the urethra of male subjects except in the area of the preprostatic urethra and in female subjects they have not been found at all. 5 In part, because of this finding, it has been suggested that parasympathetic activity is responsible for urethral smooth muscular closure. The lack of an adverse effect of sympathectomy on lower urinary tract function has been cited as further evidence that sympathetic activity is oflittle importance in lower urinary function. The demonstration that urethral smooth muscular closing function can be completely lost after extensive spinal cord injury involving the thoracolumbar sympathetic outflow indicates that urethral smooth muscular function is not autonomous and requires neural input. However, this neural participation in urethral function is unlikely to be parasympathetic in nature, since urethral functional loss was not influenced by the preservation or loss of sacral reflex activity. Indeed, the loss of urethral smooth muscular closing function in a patient with preservation of parasympathetically mediated detrusor reflex activity is strong evidence that resting urethral closure is totally independent of cholinergic influences. These findings have been duplicated experimentally and an extensive body of evidence supports the concept of sympathetic
4. 5. 6. 7.
8. 9.
observations following spinal trauma. Brit. J. Urol., 47: 161, 1975. Yalla, S. V., Blunt, K. J., Fam, B. A., Constantinople, N. L. and Gittes, R. F.: Detrusor-urethral sphincter dyssynergia. J. Urol., 118: 1026, 1977. McGuire, E. J., Wagner, F. and Weiss, R. M.: Treatment of autonomic dysreflexia with phenoxybenzamine. J. Urol., 115: 53, 1976. McGuire, E. J., Diddel, G. and Wagner, F., Jr.: Balanced bladder function in spinal cord injury patients. J. Urol., 118: 626, 1977. Gosling, J. A., Dixon, J. S. and Lendon, R. G.: The autonomic innervation of the human male and female bladder neck and proximal urethra. J. Urol., 118: 302, 1977. McGuire, E. J. and Herlihy, E.: The influence of urethral position on urinary continence. Invest. Urol., 15: 205, 1977. Awad, S. A. and Downie, J. E.: The effect of adrenergic drugs and hypogastric nerve stimulation on the canine urethra. A radiologic and urethral pressure study. Invest. Urol., 13: 298, 1976. Khanna, 0.: Disorders ofmicturition: neuropharmacologic basis and results of drug therapy. Urology, 8: 316, 1976. Saum, W. R. and De Groat, W. C.: Parasympathetic ganglia: activation of an adrenergic inhibitory mechanism by cholinomimetic agents. Science, 175: 659, 1972. EDITORIAL COMMENT
Although the conclusions of this well conducted study are based on a limited number of cases they add valuable information to our understanding of the dual role of sympathetic-parasympathetic systems in the activity of respective urethral profile components. The main statement that "resting urethral closure is totally independent of cholinergic influences" would deserve further investigation to reassess the validity of the theory that claims a cholinergic inhibitory modulating effect upon urethral smooth musculature. A.B.R.
